Diane S. Allen-Gipson, PhD, is an Instructor at the University of Nebraska Medical Center (UNMC). After her doctoral studies at Florida A&M University, Dr. Allen-Gipson completed a post-doctoral fellowshiip at UNMC and has advanced to faculty status. As an underrepresented minority, this award mechanism, Mentored Career Development Award to Promote Faculty Diversity in Biomedical Research (K01), would help Dr. Allen-Gipson advance her academic research career by providing mentoring and resources. The environment at UNMC is ideal for nurturing young scientists to academic maturity. Dr. Allen-Gipson has superior technical resources at her disposal in the new laboratory space in the state-of-the-art Durham Research Center. Likewise, intellectual resources abound ranging from academic opportunities &seminars to her mentor, Todd A. Wyatt, PhD, and co-mentor, Joseph H. Sisson, MD, and her Advisory Committee. Her research project is primed for further study. Adenosine, the metabolic breakdown product of ATP, is recognized as an important modulator of hypoxic, ischemic, and inflammatory processes critical to both tissue homeostasis and injury. Adenosine produces a wide variety of physiological effects through activation of four cell-surface receptors, A-i, AaA, A2B and A3. Through these receptors, adenosine can either protect or damage tissues depending on the receptor(s) activated. As a potent regulator of inflammation, adenosine initiates the first stage of wound-healing. If repair responses restore normal tissue architecture, function will be preserved. Our preliminary data demonstrate the multidimensional properties of adenosine in the airway, particularly in understanding receptor regulation and signaling. These findings led us to hypothesize that: Adenosine modulates airway homeostasis and wound repair. To test this hypothesis we propose the following four Specific Aims: 1. Identify the adenosine receptor(s) present on normal and wounded airway epithelium;2. Characterize and determine the effects of adenosine on airway wound healing and modulation of wound repair processes;3. Identify the signaling pathways that control adenosine-mediated homeostatic and wound repair processes in airway epithelium;and 4. Characterize the effects in vitro of adenosine- mediated epithelial homeostatic and wound repair processes using primary mouse epithelial cells. These proposed studies could lead to novel therapies for inflammatory airway diseases, such as COPD. (End of Abstract)